Two metabolic abnormalities have been found in a juvenile hypertensive syndrome. This syndrome is associated with manifestations of mineralocorticoid excess in the absence of excessive secretion of known mineralocorticoids. The metabolic abnormalities are (1) a relative defect in corticosterone 3-keto reductase with the accumulation of 4,5-dihydro metabolites, predominantly of the 5 alpha configuration, and (2) a shift of the cortisol yields (reversibly) cortisone equilibrium almost entirely in the direction of cortisol with the result that the normal metabolite, urinary free cortisone, is absent as well as the normal reduced metabolites of cortisone in urine, and the excretion of 11-keto metabolites derived from cortisone is very low. Both abnormalities lead to a prolonged cortisol metabolic clearance rate and act to enhance the efficiency of the secretion of cortisol and explain the achievement of normal plasma levels in normal glucocorticoid function in the hypertensive syndrome in the face of low cortisol secretion and excretion of metabolites.